CORTICOTROPE AND MELANOTROPE POMC-DERIVED PEPTIDES IN RELATION TO INTERRENAL FUNCTION DURING STRESS IN RAINBOW-TROUT (ONCORHYNCHUS-MYKISS)

Plasma levels of ACTH, alpha-MSH, and N-ac-beta-END, and in vitro inte rrenal ACTH sensitivity were investigated in rainbow trout (Oncorhynch us mykiss) stressed by confinement and in unstressed fish treated with exogenous cortisol. Within 3 hr after the onset of confinement, plasm a cortisol and ACTH levels were significantly elevated above control v alues, while plasma alpha-MSH, but not N-ac-beta-END, levels were sign ificantly decreased compared with those of unstressed fish. At 3 hr, s ensitivity of the interrenal tissue to ACTH stimulation in vitro was r educed in stressed fish compared to that of unstressed controls. This hyposensitivity cannot be due to the intervention of alpha-MSH or N-ac -beta-END, because after 48 hr of confinement levels of both POMC-deri ved peptides were significantly lower than in controls, whereas interr enal tissue of stressed fish still responded significantly less to an ACTH challenge than tissue from control fish. Plasma cortisol and ACTH levels in confined fish at this time point were similar to those at 3 hr. Within 96 hr of the onset of confinement, plasma ACTH levels in s tressed fish had returned to baseline levels. Plasma cortisol levels i n stressed fish at 96 hr had also declined significantly, but were sti ll higher than those in controls. The circulating cortisol level canno t be the regulatory factor responsible for the ACTH hyposensitivity ob served after 3 and 48 hr of stress, because treatment of unstressed fi sh with exogenous cortisol (which resulted in elevated plasma cortisol and lower plasma ACTH and alpha-MSH levels compared to those of contr ols) did not induce a reduction in interrenal sensitivity to ACTH. It is suggested, instead, that these data support the contention that not only the initiation of the interrenal stress response, but also the h abituation of the response, are regulated at the level of the hypothal amus via circulating ACTH levels. (C) 1995 Academic Press, Inc.